Revision Checklist Topics Flashcards

1
Q

Psoriasis - what is it and who gets it?

A

Long-lasting autoimmune disease characterised by epidermal hyperplasia and increased epidermal turnover, resulting in red, itchy and scaly patches of skin. Cause is known but largely thought to be genetic and triggered by environmental factors

Areas of the body most commonly affected: extensor surfaces (back of forearms, shins, navel area and scalp

Men and women are equally affected and the condition can arise at any age, but most commonly starts in adulthood.

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2
Q

Psoriasis - what are the different forms of this condition and how do they present?

A

Plaque (psoriasis vulgaris) - approx 90% of cases, presents with red patches and white scales on top

Guttate - drop-shaped lesions

Inverse - red patches form in skin folds

Pustular - small, non-infectious pus-filled blisters

Erythrodermic - widespread rash, can develop from any of the other types

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3
Q

Psoriasis - what changes might be seen in the body, other than the skin?

A

Nail changes - pitting, changes in colour, subungual hyperkeratosis, onycholysis

In some cases, psoriatic arthritis may also develop

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4
Q

Psoriasis - management

A

No cure, but various treatments can be employed to help control the symptoms

Steroid creams/Oral steroids

Vitamin D3 creams

UVA light treatment

Immunosuppressives e.g. methotrexate

Worsened by some medications e.g. beta-blockers, NSAIDs

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5
Q

Clinical examination of a rash - what are the three categories than need to be assessed?

A

Distribution and Configuration

  • Widespread or localised?
  • Unilateral? Bilateral? Symmetrical?
  • Which areas are affected?
  • Noticeable pattern in how the lesions are arranged?

Morphology

  • Colour
  • Size
  • Raised or flat?
  • Borders
  • Surface features e.g. scale, crust
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6
Q

Blanching and Non-blanching rashes - what is the term given to a non-blanching rash? Why does it not blanch? Name one very important condition that presents with a non-blanching rash

A

Purpura - a purpuric rash is one that does not blanch due to extravasation of blood

Meningitis presents with a non-blancing rash

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7
Q

What terms are used to describe flat lesions?

What term is given to a rash that is completely flat?

A

Macule if <1cm

Patch if >1cm

A macular rash

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8
Q

What terms are used to describe raised lesions?

What term is used to describe a rash that is elevated?

How about if a rash has areas that are both flat and elevated?

A

Papule if the elevated area is <0.5cm

Nodule if the elevated area is >0.5cm

A papular rash is one that is raised

If a rash has both flat and elevated areas, it is termed maculopapular

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9
Q

Give some of the different types of nodule that may occur in a raised rash

A

Plaque - raised edge and flatter surface

Wheal - compressible dermal swelling

Vesicles and Bullae - fluid-filled

Cyst - nodule containing semi-solid material

Pustule - contains pus

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10
Q

Define the following terms…

  • Hyperkeratosis
  • Parakeratosis
  • Acanthosis
A

Hyperkeratosis - increased thickness of the keratin layer

Parakeratosis - persistence of nuclei in the keratin layer

Acanthosis - thickening of the whole epidermis

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11
Q

From superficial to deep, what are the four layers of the epidermis?

A

Keratin layer

Granular Layer

Prickle Cell Layer

Basal cell layer

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12
Q

Eczema (aka dermatitis) - what is the common feature of all eczema cases?

What are the two phases of eczema? List some features of each stage

A

Itch! Common feature of all eczemas

Acute phase - papulovesicular, red (erythematous) lesions, oedema (spongiosis) and ooze or scaling and crusting

Chronic phase - thickening (lichenification), elevated plaques, increased scaling

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13
Q

Name some forms of dermatitis (7)

A

Contact allergic - delayed (Type IV) hypersensitivity

Contact irritant - trauma e.g. soap, water etc.

Atopic - genetic and environmental factors

Drug-related - Type I or Type IV hypersensitivity

Photo-induced/photo-sensitive - reaction to UV light

Lichen simplex - caused by physical trauma to skin e.g. scratching

Stasis - caused by physical trauma to skin e.g. hydrostatic pressure due to stasis of blood

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14
Q

Contact dermatitis - very briefly describe the pathophysiology of this condition

A

Upon antigen challenge, specifically sensitised T cells proliferate and migrate to the skin, resulting in inflammation = dermatitis

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15
Q

Contact dermatitis - how is this condition tested for?

A

Patch testing

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16
Q

How to contact allergic and contact irritant forms of dermatitis differ from one another?

A

Contact irritant is due to non-specific physical irritation rather than a specific allergic reaction

These two conditions may be difficult to distinguish from one another, and the two may co-exist

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17
Q

Atopic eczema - signs and symptoms

A

Pruritus (itch)

Ill-defined erythema and scaling

Generalised dry skin

Flexor surface distribution

Associated with other atopic diseases e.g. asthma, allergic rhinitis, food allergies etc.

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18
Q

Atopic eczema - what chronic changes may be seen in this condition?

What does crusting indicate?

A

Lichenification

Excoriation

Secondary infection. Crusting indicates Staph aureus infection

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19
Q

Atopic eczema - what infectious organism may cause secondary infection in someone with atopic eczema that results in “monomorphic punched-out lesions”?

A

Herpes simplex virus causing Eczema herpeticum

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20
Q

Atopic eczema - how is this condition diagnosed?

A

Itching plus 3 or more of the following…

  • visible flexural rash
  • history of flexural rash
  • personal history of atopy
  • generally dry skin
  • onset before 2 years old
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21
Q

Atopic eczema - what gene appears to be especially important in the development of this condition?

A

FLG gene encoding for Filaggrin

22
Q

Atopic eczema - management

A

Plenty of emollients

Avoid irritants

Topical steroids

Treat secondary infections

Phototherapy - mainly UVB

Systemic immunosuppressants if need be

(Biologic agents…)

23
Q

Define ‘spongiosis’

A

Oedema in the keratin layer of the epidermis, between the keratinocytes

24
Q

What are the 4 reaction patterns seen in inflammatory skin diseases?

A

Spongiotic-intraepidermal oedema

Psoriasiform - elongation of the rete ridges e.g. psoriasis

Lichenoid - basal layer damage e.g. lichen planus, SLE

Vesiculobullous - blistering e.g. pemphigus, pemphigoid

25
Q

Pemphigus - what is it?

A

Rare autoimmune bullous disease

Loss of integrity of epidermal cell adhesion - fault is at DEJ

4 distinct subtypes, with 80% of cases being Pemphigus vulgaris

26
Q

Pemphigus vulgaris - what type of immunoglobulin is involved, and what does it target?

What is the end result?

A

IgG

Made against Desmoglein-3 - maintains desmosomal attachments

End result is acantholysis

27
Q

Pemphigus vulgaris - clinical presentation, and what the key difference is between it and bullous pemphigoid

A

Involves skin especially scalp, face, axillae, groin and trunk

May also affect the mucosa in the mouth and resp tract

Result is fluid-filled blisters which rupture to form shallow erosions

Crucially, bullous pemphigoid blisters are subepidermal and there is no evidence of acantholysis

28
Q

Bullous pemphigus - what is the immunological target in this condition?

What needs to be kept in mind when sending lesions for histology?

A

IgG attacks hemidesmosomes anchoring basal cells to the basement membrane

Early lesions need to be sent for histoloy as later lesions show re-epithelialisation and hence mimick pemphigus vulgaris

29
Q

Dermatitis herpetiformis - presentation

A

Autoimmune bullous disease - relatively rare

Intensely itchy summetrical lesions

Elbows, knees and buttocks affected, often lesions are excoriated

Hallmark is papillary dermal microabscesses

30
Q

Dermatitis herpetiformis - what disease is this condition strongly associated with?

What HLA type is this disease strongly associated with?

A

Disease - Coeliac disease, 90% have gluten sensitive enteropathy

HLA type - HLA-DQ2

31
Q

Acne vulgaris - common sites of presentation and aetiology (including bacterial species)

A

Sites of presentation

  • face
  • upper back
  • anterior chest
  • (distribution reflects sebaceous glands)

Aetiology

  • Increased androgens at puberty
  • Increased androgen sensitivity of sebaceous glands (maybe?)
  • Keratin plugging of pilosebaceous units
  • Infection with anaerobic bacterium - Corynebacterium acnes
32
Q

Rosacea - presentation

A

Common condition, affecting approx. 10% of caucasian adults

More commonly seen in females

Recurrent facial flushing

Visible blood vessels

Pustules - NO comedones

Thickening of the skin - rhinophyma (large red bumpy nose)

33
Q

Rosacea - triggers

A

Sunlight

Alcohol

Spicy foods

Stress

Allergic reaction to mites?

34
Q

What are the 4 main groups of porphyrias?

A

Phototoxic skin porphyrias e.g. porphyria cutanea tarda (PCT), erythropoetic protoporphyria (EPP)

Blistering and fragile skin porphyrias

Acute attack porphyrias

Severe congenital porphyrias e.g. congenital erythropoetic porphyria

35
Q

Porphyria Cutanea Tarda (PCT) Type I - what enzyme is defective? What does this result in a build up of?

A

Defective enzyme - Uroporphyrinogen decarboxylase

Build up of Uroporphyrinogen III

36
Q

Porphyria Cutanea Tarda - typical presentation and diagnosis

A

Most common phototoxic skin porphyria

Blisters

Fragility

Others - hyperpigmentation, hypertrichosis (excessive hair growth), solar urticaria (hives), morphoea (painless discoloured patches)

Diagnosis - typically done using a Woods lamp test, and also spectrofluorometers

37
Q

PCT - management

A

Having established PCT, now need to establish the underlying cause…

  • alcohol
  • viral hepatitis
  • oestrogens
  • haemochromatosis

Then treatment aims to relieve the skin disease and treat the underlying cause

38
Q

Erythropoietic protoporphyria (EPP) - reduced activity in what enzyme brings about this condition, and what does this lead to a build up of?

A

Reduced activity - Ferrochelatase

Build up of Protoporphyrin IX

39
Q

EPP - presentation

A

Usually presents in childhood with most common presentation being acute photosensitivity of skin

A few minutes of sun exposure can produce pruritius, erythema, swelling and pain

After chronic exposure patients may develop lichenification, hypo/hyperpigmentation and scarring

40
Q

EPP - investigations

A

Porphyrin plasma scan is best

Can also look for fluorocytes, transaminases, Hb levels etc.

41
Q

EPP - management

A

Explain the diagnosis to the patient and arrange for LFTs and RBC porphyrins to be screened every 6 months - this is because EPP can potentially result in Liver Failure

Visible light photoprotection measures should be taken e.g. behavioural, clothing, topical sunscreen etc.

42
Q

Acute Intermittent Porphyria - what enzyme is reduced in activity and what does this lead to a build up of?

A

Reduced activity - PBG deaminase

Build up of Porphobilinogen (PBG)

43
Q

Acute Intermittent Porphyria - signs and symptoms

A

Severe and poorly localised abdominal pain is very common

Urinary signs - painful urination, urinary retention or incontinence, darkened urine etc.

Other very general signs - anxiety, depression, nausea, vomiting, headache, tachycardia, hypertension etc.

44
Q

What is the most common type of drug eruption? What other types are there?

A

Most common - exanthematous drug eruption (90%)

Urticarial (5-10%)

Papulosquamous/pustular/bullous

Also pigmentation, itch/pain, photosensitivity

45
Q

What kind of hypersensitivity is an exanthematous drug eruption?

How does it present?

A

Type IV - delayed and T-cell mediated

Usually mild and self-limiting, symmetrical widespread rash

Itch and mild fever are common

Onset is 4-21 days after first taking the drug

46
Q

What features might suggest that an exanthematous drug eruption is potentially severe?

A
  • Involvement of the mucous membranes and the face
  • Facial oedema and erythaema
  • Fever
  • Blisters, purpura and necrosis
  • Lymphadenopathy, arthralgia
  • SoB, wheezing
47
Q

List some of the drugs associated with erythematous drug eruptions

A

Penicillins

Sulphonamide antibiotics

Erythromycin

Streptomycin

Allopurinol

NSAIDs

Phenytoin

Chloramphenicol

48
Q

What kind of hypersensitivity reaction is an urticarial drug eruption?

A

Type I - IgE-mediated allergic reaction

49
Q

List some types of pustular/bullous drug eruptions and what medications might cause them

A

Acne

  • Glucocorticoids
  • Androgens, lithium, isoniazid, phenytoin

Acute Generalised Exanthematous Pustulosis (AGEP) - rare

  • Antibiotics
  • CCBs
  • Antimalarials

Drug-enduced Bullous Pemphigoid

  • ACE inhibitors
  • Penicillin
  • Furosemide
50
Q

Severe Cutaneous Adverse reactions can be life threatening! Name some of these conditions

A

Steven-Johnson Syndrome

Toxic Epidermal Necrolysis

Drug reaction with eosinophilia and systemic symptoms (DRESS)

Acute Generalised Exanthematous Pustulosis (AGEP)